COBALT-RELATED ASTHMA - CLINICAL AND IMMUNOLOGICAL ASPECTS

Several clinical and experimental findings point to cobalt as the only sensitizer and causal agent of hard metal asthma. The clinical features have been clearly defined by bronchial provocation tests, with a prevalence of late phase responses. Epidemiology is still insufficient to configure prevalence and incidence rates for cobalt asthma. IgE and IgG antibodies with cobalt specificity have been demonstrated, but T-lymphocytes and eosinophyls involvement seem to be important in the mechanism of an allergic inflammation in the airways. Such an immunological pathogenesis links cobalt asthma with other manifestation of hard metal disease.